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Biomedical subjects

S Noma

Publications and source records attributed to S Noma.

At least 73 records · Page 4Linked to original sources
PubMed1986

Centrilobular lesions of the lung: demonstration by high-resolution CT and pathologic correlation.

To determine the value of high-resolution computed tomography (HRCT) in the diagnosis of diffuse pulmonary diseases, a direct HRCT-pathologic correlative study was performed using four inflated and fixed lungs from autopsy. In normal lungs, the smallest pulmonary artery resolved by HRCT was 200 microns in diameter; the artery was accompanied by the terminal bronchiole and the first-order respiratory bronchiole. The distance from the vessel to the corresponding lobular border ranged from 3 to 5 mm. These results suggest that the centrilobular area or the area around the terminal or respiratory bronchioles can be recognized with HRCT. In addition, the authors confirmed that centrilobular emphysema and centrilobular tuberculous nodules can be diagnosed with HRCT. Thus, HRCT can demonstrate the location of pathologic changes within a lobule and may be helpful in the differential diagnosis of diffuse pulmonary diseases.

Humans↗
PubMed1986

Effects of apomorphine on morphine analgesia during the state of dopaminergic supersensitivity after chronic treatment with haloperidol.

Morphine induced-reduction in response to a repetitive electrical stimulation of the tail was measured in acute rats and rats chronically treated with haloperidol (1 mg/kg/d, for 7 d) following pretreatment with apomorphine. In acute experiments, a significant enhancement of the anti-struggling action of morphine was produced by haloperidol (1 mg/kg, i.p.). Low doses of apomorphine (30-480 micrograms/kg, i.p.) had no influence on the suppressing action of morphine on the struggling response induced by the tail stimulation. Following chronic treatment with haloperidol, the inhibitory action of morphine on the tail stimulation-induced struggling response was dose-dependently inhibited by very low doses of apomorphine (60-480 micrograms/kg, i.p.). A significant increase in 3,4-dihydroxyphenylacetic acid (DOPAC) levels was observed after administration of haloperidol or morphine in acute rats, whereas no change in DOPAC levels was found after administration of morphine or apomorphine in chronically haloperidol-treated rats. In these animals, basal striatal DOPAC levels were significantly decreased compared with those of vehicle-treated animals controls. The present results suggest that in rats treated chronically with haloperidol, the suppressive action of a low dose of apomorphine on morphine analgesia is due to an increased sensitivity of postsynaptic dopaminergic receptors to apomorphine.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

Effects of eperisone applied by microiontophoresis on neurons in the medial and lateral vestibular nuclei.

Electrophysiological studies were performed to elucidate the mechanism underlying the antivertigo action of eperisone, an antispastic drug, using cats anesthetized with alpha-chloralose. Iontophoretic application of eperisone up to 100 nA produced a dose-dependent inhibition of spike generation upon vestibular nerve stimulation in monosynaptic and polysynaptic neurons of the medial vestibular nucleus (MVN). The inhibition of neurons in the MVN was more prominent than that in the lateral vestibular nucleus. In addition, iontophoretically applied eperisone in doses of 50-100 nA inhibited the orthodromic spike elicited by vestibular nerve stimulation in the MVN monosynaptic neurons projecting to the abducens nucleus (ascending neuron), without affecting that in the MVN neurons projecting to the spinal cord (descending neuron). An inhibition of antidromic spike elicited by abducens nucleus stimulation in the MVN monosynaptic ascending neurons was observed in some cases during application of eperisone. These results suggest that eperisone predominantly inhibits synaptic transmission of the MVN ascending neurons.

Animals↗
PubMed1985

Changes in left ventricular diastolic function after left ventriculography: a comparison with iopamidol and urografin.

Changes in left ventricular (LV) diastolic indices after left ventriculography (LVG) with iopamidol or urografin were studied in 42 subjects. Increase in heart rate and decrease in LV systolic pressure were more significant with urografin than with iopamidol (p less than 0.05 to 0.001). LV end-diastolic pressure was elevated more with urografin than with iopamidol (p less than 0.005 to 0.05) 1 to 3 minutes after LVG. LV peak negative dP/dt decreased significantly with urografin immediately (10 to 15 seconds, -511 and 30 seconds, -376 mm Hg/sec; p less than 0.0005 to 0.02), but with iopamidol it did not decrease significantly after LVG. Time constant, T, was elongated with iopamidol (10 to 15 seconds, +13 and 30 seconds, +6 msec; p less than 0.0005), but this elongation was significantly less than urografin (10 to 15 seconds, +34; 30 seconds, +25; 1 minute, +15; and 2 minutes, +10 msec; p less than 0.05 to 0.0005). We conclude that iopamidol disturbed LV diastolic function to a lesser degree than did urografin.

Adult↗
PubMed1984

Assay for catechol-O-methyltransferase in erythrocytes using a new fluorogenic substrate, 2-(3,4-dihydroxyphenyl)naphtho[1,2-d]thiazole.

A highly sensitive method for the assay of catechol-O-methyltransferase in erythrocytes is described, which employs high-performance liquid chromatography with fluorescence detection. A newly synthesized catechol compound, 2-(3,4-dihydroxyphenyl)naphtho [1,2-d]thiazole is used as a highly fluorogenic substrate for catechol-O-methyltransferase; the m- and p-methylated products formed enzymatically from the substrate under the optimum conditions, after extraction with n-hexane--chloroform, are separated by normal-phase chromatography on LiChrosorb Si 100. The limits of detection for m- and p-methylated products are 3 pmol per assay tube (60 fmol per injection volume of 20 microliter) in each case. The ratio of m- and p-methylated products was 0.54. This method requires as little as 50 microliter of human erythrocytes.

Benzothiazoles↗
PubMed1984

[Apical hypertrophy as a part of the morphologic spectrum of hypertrophic cardiomyopathy].

Clinical and morphological features in 10 cases of "apical hypertrophic cardiomyopathy" (apical type) were analyzed and compared with those in classic hypertrophic cardiomyopathy with asymmetric septal hypertrophy (ASH). The hypertrophic pattern of the interventricular septum (IVS) was evaluated on the two-dimensional echocardiographic (2-D) left ventricular (LV) long-axis view. Thirty-one of 70 patients with ASH were characterized by predominant hypertrophy of the basal IVS (Type I). Seventeen patients had predominant hypertrophy of the apical IVS (Type III). Diffuse IVS hypertrophy was noted in 22 patients (Type II). Electrocardiographic similarity was documented between cases with Type III and apical type; that is, a low incidence of abnormal Q waves, a high incidence of giant negative T waves, and frequent absence of Q waves. In Type I and II, abnormal Q waves were frequently observed, while giant negative T waves were rare. On the 2-D LV short-axis view at the papillary muscle level, three groups with ASH revealed similar distributions of myocardial hypertrophy characterized by extension of hypertrophy to the LV anterior free all and papillary muscles. Most cases with apical type had a similar distribution of hypertrophy, but its degree was significantly less severe than that of ASH. Comparison of diastolic LV configurations on left ventriculograms and/or the 2-D apical two-chamber views indicated the morphologic continuity among the three types with ASH and the apical type. Clinical features in cases of the apical type were obviously less severe than those of three groups with ASH, as indicated by a significantly larger proportion of asymptomatic patients (90%), absence of sudden death and rare documentation of malignant ventricular arrhythmias on 24-hours ambulatory electrocardiography. In conclusion, apical type can be categorized as a part of hypertrophic cardiomyopathy with a wide morphologic spectrum rather than the separate disease entity, and it is characterized by giant negative T waves with minimum clinical manifestations.

Cardiac Catheterization↗
PubMed1983

Pattern of myocardial hypertrophy as a possible determinant of abnormal Q waves in hypertrophic cardiomyopathy.

Echocardiographic and electrocardiographic findings in 74 adults with hypertrophic cardiomyopathy (HCM) were analyzed to identify the pattern of myocardial hypertrophy as a possible determinant of abnormal Q waves. The pattern of septal hypertrophy along the left ventricular long axis was divided into 3 types based on the site of maximum septal hypertrophy: basal, diffuse and apical types. Abnormal Q waves defined by the revised Minnesota Codes (either I-I, I-II or I-III) were noted in 31 cases (42%). The total incidence of abnormal Q waves in the basal type (15/26, 58%) and in the diffuse type (12/22, 55%) was significantly higher (p less than 0.001 and p less than 0.01, respectively) than that in the apical type (4/26, 15%). The abnormal Q waves defined by the strict criteria of Code I-I were significantly more prevalent (p less than 0.05) in the basal type than in the diffuse type, although there was no significant difference in the total incidence of abnormal Q waves between these 2 groups. Thirty-six patients with an extension of hypertrophy to the right ventricle (RVH) had a significantly higher incidence of abnormal Q waves than 22 patients without RVH (56% vs 27%, p less than 0.05). Furthermore, close relationships of RVH to the location of abnormal Q waves were documented. In conclusion, the abnormal Q waves in HCM may be related to the pattern of septal hypertrophy along the left ventricular long axis and to RVH.

Adult↗
PubMed1982

Differential effects of alpha-, beta- and gamma-endorphins on dopamine metabolism in the mouse brain.

The effects of intracerebral injection of alpha-, beta- and gamma-endorphins on the mouse brain dopamine (DA) metabolism were contrasted in relation to the previously identified patterns of behavior. alpha-Endorphin (20 micrograms) decreased the content of homovanillic acid (HVA) in the striatum, while gamma-endorphin (10 micrograms) the contents of DA, 3,4-dihydroxyphenylacetic acid and HVA. beta-Endorphin (1 and 2 micrograms) had no effects on the mouse DA metabolism in the brain. The changes in the DA metabolism induced by alpha- and gamma-endorphins were readily reversed by the pretreatment with naloxone (1 mg/kg). Results suggested: (1) the patterns of behavior in mice treated with endorphins are mediated by these differences in DA metabolism; (2) changes in DA metabolism induced by alpha- and gamma-endorphins occur via opiate receptors in the mouse brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

[Echocardiographic findings of a patient with cardiac amyloidosis and left ventricular outflow obstruction].

This report described 56-year-old male with cardiac amyloidosis, whose echocardiographic and hemodynamic findings suggested hypertrophic obstructive cardiomyopathy. M-mode echocardiography demonstrated asymmetric septal hypertrophy (2.1 cm/1.6 cm), systolic anterior motion of the mitral valve, and pericardial effusion. Two-dimensional echocardiography revealed marked hypertrophy of the septum and papillary muscles with characteristic fine grannular sparkling appearance of the myocardium. Bilateral heart catheterization showed normal hemodynamics except a pressure gradient of 35 mmHg within the left ventricular outflow tract. Moreover, no hemodynamic evidence of restrictive cardiomyopathy was observed. Myocardial biopsy was performed at the time of pericardiectomy, and diffuse amyloid deposits were identified between myocardial fibers. It is of particular interest that cardiac amyloidosis presented the form of ventricular hypertrophy associated with left ventricular outflow obstruction, probably due to uneven deposition of amyloid.

Amyloidosis↗
PubMed1982

Determination of methionine-enkephalin, norepinephrine, dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxy-4-hydroxyphenylacetic acid (HVA) in brain by high-pressure liquid chromatography with electrochemical detector.

High-pressure liquid chromatography with electrochemical detection is utilized in a procedure for the determination of methionine-enkephalin (MET-ENK), norepinephrine (NE), dopamine (DA), 3, 4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxy-4-hydroxyphenylacetic acid (HVA) in same brain tissue samples. The high degree of selectivity and sensitivity (picomole limits for each component) makes this technique directly applicable to extremely small samples. After optimal conditions had been established, the procedure was employed in the determination of MET-ENK, NE, DA, DOPAC and HVA contents in whole brains, 7 discrete brain areas of mice and rats.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1981

[Psychopharmacological study of enkephalins, with special reference to the relation between behavioral profiles and brain monoamines].

The effects of intracerebral injection of methionine-enkephalin (met-enk) and leucine-enkephalin (leu-enk) on the behavioral patterns were examined by using multi-dimensional behavioral analyser (Animex II) in relation to the mouse brain monoamine metabolism. The multi-dimensional behavioral analyser which is able to record 9 different measures of behavior exhibited by mice has been used. The results have indicated that met-enk (100 micrograms) and leu-enk (200 micrograms) caused a remarkable but transient increase in the linear locomotion recorded on the counter 1/1. In the biochemical study, it has been found that met-enk (100 micrograms) significantly increases the content of homovanillic acid (HVA) in the striatum. Leu-enk (200 micrograms) has negligible effect on the contents of dopamine (DA), 3,3-hydroxyphenylacetic acid and HVA in the cerebral cortex or the striatum. Met-enk (100 micrograms) and leu-enk (200 micrograms) did not affect the alpha-methyl-p-tyrosine-induced decrease in the content of DA and norepinephrine. Following the injection of met-enk (100 micrograms) and leu-enk (200 micrograms) and leu-enk (200 micrograms) into the cerebral ventricle, the content of 5-hydroxytryptamine in the cerebral cortex was increased but that of 5-hydroxyindoleacetic acid was not. Neither met-enk nor leu-enk influenced the activity of monoamine oxidase in the brain. These data suggest that, while monoamines in the brain are involved in the behavioral effects of enkephalins, the precise sites and/or mechanisms of enkephalins may differ.

Animals↗